GI and Liver Flashcards
1
Q
how can you differentiate biliary colic from acute cholangitis
A
In contrast to acute cholecystitis, there is no fever and inflammatory markers are normal in biliary colic
2
Q
what is charcot’s triad
A
- it is
- right upper quadrant pain
- fever
- jaundice
- it’s for ascending cholangiti
- it occurs in ~20-50% of people with ascending cholangitis
3
Q
is pain from duodenal ulcers or gastric ulcers made worse by eating
A
Duodenal ulcers: more common than gastric ulcers, epigastric pain relieved by eating
Gastric ulcers: epigastric pain worsened by eating
4
Q
what is rovsing’s sign?
A
more pain in RIF than LIF when palpating LIF
it indicates appendicitis
5
Q
when would you get tinkling bowel sounds
A
if there is intestinal obstruction
6
Q
how does the pain differ between renal colic and acute pyelonephritis
A
- renal colic:
- Pain is often severe but intermittent. Patient’s are characteristically restless
- Visible or non-visible haematuria may be present
- acute pyelonephritis:
- Fever, vomiting and rigors
7
Q
what is the most common causative organism in ascending cholangitis
A
E. coli
8
Q
what is reynold’s pentad for ascending cholangitis
A
- it’s charcot’s triad:
- fever
- RUQ pain
- jaundice
- plus hypotension and confusion
it’s for ascending cholangitis
9
Q
how do you diagnose ascending cholangitis
A
ultrasound is generally used first-line in suspected cases to look for bile duct dilation and bile duct stones
bloods will show raised white cells and raised inflammatory markers
10
Q
what is the management of ascending cholangitis
A
intravenous antibiotics
endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction
11
Q
clincal features of acute pancreatitis
A
severe epigastric pain that may radiate through to the back
vomiting is common
examination may reveal epigastric tenderness, ileus and low-grade fever
periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare
12
Q
how do you diagnose pancreatitis
A
a diagnosis of acute pancreatits can be made without imaging if characteristic pain + amylase/lipase > 3 times normal level
however, early ultrasound imaging is important to assess the aetiology as this may affect management - e.g. patients with gallstones/biliary obstruction
13
Q
what are the two important blood tests for pancreatitis
A
- serum amylase
- raised in 75% of patients
- typically > 3 times the upper limit of normal in pancreatitis
- levels do not correlate with disease severity
- specificity about 90%
- serum lipase
- more sensitive and specific than serum amylase
14
Q
what are the non-pancreatitis causes of raised amylase
A
pancreatic pseudocyst
mesenteric infarct
perforated viscus
acute cholecystitis
diabetic ketoacidosis
15
Q
what are some poor prognostic factors in pancreatitis
A
- age > 55 years
- hypocalcaemia
- hyperglycaemia
- hypoxia
- neutrophilia
- elevated LDH and AST
16
Q
what are the causes of pancreatitis
A
- GETSMASHED
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps (other viruses include Coxsackie B)
- Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
- Scorpion venom
- Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
- ERCP
- Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)
17
Q
how do you classify the severity of pancreatitis
A
18
Q
management of pancreatitis
A
- fluids
- aggressive early rehydration with crystalloids
- aim for urine output of 0.5ml/kg/hr
- may relieve pain by treating lactic acidosis
- analgesia
- IV opioids
- nutrition
- don’t make them nil by mouth unless they are vomiting
- enteral nutrition should be offered to anyone with moderately severe or severe acute pancreatitis within 72 hours of presentation
- parenteral nutrition only used if enteral fails
- surgery
- if due to gallstones then cholecystectomy
- if obstructed biliary system due to stones then ERCP
- if infected necrosis then either radiological drainage or surgical necrosectomy.
19
Q
what is the main cause of chronic pancreatitis
A
- 80% of cases are due to excess alcohol use
- 20% of cases are due to:
- genetic: cystic fibrosis, haemochromatosis
- ductal obstruction: tumours, stones,
20
Q
clinical features of chronic pancreatitis
A
- pain is typically worse 15 to 30 minutes following a meal
- steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
- diabetes mellitus develops in the majority of patients typically more than 20 years after symptom begin
21
Q
how do you investigate chronic pancreatitis
A
- CT shows pancreatic calcification
- faecal elastase detects pancreatic exocrine function
22
Q
management of chronic pancreatitis
A
pancreatic enzyme supplementation
analgesia
23
Q
is there a vaccine for hepatitis C
A
no
24
Q
what is the investigation to diagnose hepatitis C
A
HCV RNA
25
is hepatitis C acute or chronic
* around 15-45% of patients will clear the virus after an acute infection (depending on their age and underlying health) and hence the majority (55-85%) will develop chronic hepatitis C
26
what is the definition of chronic hepatitis C
the persistence of HCV RNA in the blood for 6 months.
27
complications of chronic hepatitis C infection
* cirrhosis
* hepatocellular carcinoma
* membranoproliferative glomerulonephritis
* sjorgen's syndrome
28
how do you manage hepatitis C
* daclatasvir + sofosbuvir or sofosbuvir + simeprevir with or without ribavirin
* aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
29
what are the side effects of ribavirin
haemolytic anaemia
cough
Women should not become pregnant within 6 months of stopping ribavirin as it is teratogenic
30
what is hepatitis D and B coinfection
A patient is infected with hepatitis B and hepatitis D at the same time
31
what is hepatitis B and D superinfection
A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection
Superinfection is associated with high risk of fulminant hepatitis, chronic hepatitis status and cirrhosis.
32
what is the treatment for hepatitis B
pegylated interferon-alpha
33
important things to remember about hep E
* faecal oral route
* incubation period is 3-8 weeks
* common in Central and South-East Asia, North and West Africa, and in Mexico
* causes significant mortality in pregnancy (20%)
* does not cause chronic disease
34
how long is the incubation period for hepatitis A
2-4 weeks
35
what are the clinical features of hepatitis A
* flu-like prodrome
* abdominal pain: typically right upper quadrant
* tender hepatomegaly
* jaundice
* cholestatic liver function tests
* faecal-oral spread
* doesn't cause chronic disease
* benign, self-limiting disease
36
who should be vaccinated against hepatitis A
* an effective vaccine is available
* after the initial dose a booster dose should be given 6-12 months later
* people travelling to or going to reside in areas of high or intermediate prevalence, if aged \> 1 year old
* people with chronic liver disease
* patients with haemophilia
* men who have sex with men
* injecting drug users
37
how will lfts be deranged in alcoholic liver disease
* cGamma-GT will be raised
* the AST-ALT ration will be \>2
* if it's \>3 then this is strongly suggestive of acute alcoholic hepatitis
38
what can be used to treat alcoholic hepatitis
prednisolone
39
which weird blood test can show hepatocellular carcinoma
raised AFP can be a useful diagnostic marker of HCC
40
Who should be screened for hepatocellular carcinoma and how
* Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:
* patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
* men with liver cirrhosis secondary to alcohol
41
a serum-ascites albumin gradient above what level is indicative of portal hypertension
11g/L
42
what are some causes of a serum-ascites albumin gradient \>11g/L
* Liver disorders are the most common cause
* cirrhosis/alcoholic liver disease
* acute liver failure
* liver metastases
* Cardiac
* right heart failure
* constrictive pericarditis
* Other causes
* Budd-Chiari syndrome
* portal vein thrombosis
* veno-occlusive disease
* myxoedema
43
what is saag
serum-asites albumin gradient
SAAG = ([serum](https://en.wikipedia.org/wiki/Blood_serum) [albumin](https://en.wikipedia.org/wiki/Albumin)) − (albumin level of ascitic fluid).
44
what are some causes of saag \<11g/L
* Hypoalbuminaemia
* nephrotic syndrome
* severe malnutrition (e.g. Kwashiorkor)
* Malignancy
* peritoneal carcinomatosis
* Infections
* tuberculous peritonitis
* Other causes
* pancreatitisis
* bowel obstruction
* biliary ascites
* postoperative lymphatic leak
* serositis in connective tissue diseases
45
management of ascites
* sodium restriction
* if sodium \<124 then consider fluid restriction
* spironolactone +/- loop diuretic
* therapeutic paracentesis of tense ascites
* if \>5L then give albumin cover to prevent paracentesis induced circulatory dysfunction
* transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
46
which patients with ascites should get prophylactic antibiotic cover and what should they have
*prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved*
47
how do you diagnose spontaneous bacterial peritonitis
* paracentesis
* neutrophil count \>250 cells/uL
48
what is the most common causative organism in spontaneous bacterial peritonitis
e.coli
49
what is the best antibiotic for spontaneous bacterial peritonitis
IV cefotaxime
50
what is the pathophysiology of acute colecystitis
* develops secondary to gallstones in 90% of patients (acute calculous cholecystitis)
* the remaining 10% of cases are referred to as acalculous cholecystitis
* typically seen in hospitalised and severely ill patients
* multifactorial pathophysiology: gallbladder stasis, hypoperfusion, infection
* in immunosuppressed patients it may develop secondary to *Cryptosporidium* or cytomegalovirus
* associated with high morbidity and mortality rates
51
what is the first line investigation for acute cholecystitis
* ultrasound is the first-line investigation of choice
* if the diagnosis remains unclear then cholescintigraphy (HIDA scan) may be used
* technetium-labelled HIDA (hepatobiliary iminodiacetic acid) is injected IV and taken up selectively by hepatocytes and excreted into bile
* in acute cholecystitis there is cystic duct obstruction (secondary to odema associated with inflammation or an obstructing stone) and hence the gallbladder will not be visualised
52
what is the treatment for acute cholecystitis
iv antibiotics and early laparoscopic cholecystectomy within 1 week of diagnosis
53
risk factors for gallstones
* Fat
* Female
* Fertile (pregnancy and COCP)
* Forty
* also
* diabetes
* crohns
* rapid weightloss (i.e. from bariatric surgery)
54
what is the pain in biliary colic caused by
gallstones passing through the biliary tree
or due to the gallbladder contracting around a stone
55
features of biliary colic
* colicky right upper quadrant pain
* worse after eating
* may radiate to back, between scapulae
* nausea and vomiting
* LFTs are NORMAL
* unless it's in the CBD
* NO FEVER
* Inflammatory markers are NORMAL
56
complications of gallstones
* acute cholecystitis: the most common complication
* ascending cholangitis
* acute pancreatitis
* gallstone ileus
* gallbladder cancer
57
management of cholangitis
* Fluid resuscitation
* Broad-spectrum intravenous antibiotics
* Correct any coagulopathy
* Early ERCP
58
how do you manage asymptomatic gallstones
* if in gallbladder then manage expectantly since they rarely cause problems
* if in cbd then consider surgical managment
59
what are the two scores for severity of liver cirrhosis
* Child-Pugh score
* Model for end stage liver disease (MELD)
60
what are the risks of ERCP
* bleeding
* cholangitis
* perforation
* pancreatitis
61
What is the model for end stage liver disease
Uses a combination of a patient's bilirubin, creatinine, and the international normalized ratio (INR) to predict survival. A formula is used to calculate the score.
formula is quite long and boring don't learn it
62
how do you diagnose liver cirrhosis
* transient elastography
* brand name 'Fibroscan'
* uses a 50-MHz wave is passed into the liver from a small transducer on the end of an ultrasound probe
* measures the 'stiffness' of the liver which is a proxy for fibrosis
63
what further investigations should you do for people with liver cirrhosis?
* Upper endoscopy to check for varices in patient's with a new diagnosis of cirrhosis
* liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer
64
what is the child pugh classification
* it's for staging liver cirrhosis
65
which HLA types is coeliac associated with
HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).
66
should coeliac testing be done while the patient is taking gluten or not
patients should reintroduce gluten for at least 6 weeks prior to testing.
67
what serology can you do for coeliac
* tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
* endomyseal antibody (IgA)
* needed to look for selective IgA deficiency, which would give a false negative coeliac result
68
what is the gold standard for diagnosis of coeliac
* endoscopic intestinal biopsy (duodenum or jejumum):
* villous atrophy
* crypt hyperplasia
* increase in intraepithelial lymphocytes
* lamina propria infiltration with lymphocytes
69
apart from being gluten free what do coeliac patients need
* they might have functional hyposplenism
* For this reason, they're offered the pneumococcal vaccine
* and a booster every 5 years
70
first-line pharmacological treatment of IBS
* pain: antispasmodic agents
* constipation: laxatives but avoid lactulose
* diarrhoea: loperamide is first-line
71
what is the second line treatment of IBS
low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg)
72
what is the difference between diverticulosis, diverticulitis and diverticular disease
* diverticulosis: outpouchings present without symptoms
* diverticular disease: symptoms present
* diverticulitis: infection of the diverticula
73
symptoms of diverticular disease
* Altered bowel habit
* rectal bleeding
* Abdominal pain
74
complications of diverticular disease
* Diverticulitis
* Haemorrhage
* Development of fistula
* Perforation and faecal peritonitis
* Perforation and development of abscess
* Development of diverticular phlegmon
75
diverticulitis investigation
* FBC: raised WCC
* CRP: raised
* Erect CXR: may show pneumoperitoneum in cases of perforation
* AXR: may show dilated bowel loops, obstruction or abscesses
* CT: this is the best modality in suspected abscesses
* Colonoscopy: should be avoided initially due to increased risk of perforation in diverticulitis
76
management of diverticulitis
* mild cases of acute diverticulitis may be managed with oral antibiotics, liquid diet and analgesia
* if the symptoms don't settle within 72 hours, or the patient intiially presents with more severe symptoms, the patient should be admitted to hospital for IV antibiotics
77
if patients with dyspepsia don't meet criteria for referral then how do you treat them
* 1. Review medications for possible causes of dyspepsia
* 2. Lifestyle advice
* 3. Trial of full-dose proton pump inhibitor for one month OR a 'test and treat' approach for *H. pylori*
* if symptoms persist after either of the above approaches then the alternative approach should be tried
78
which patients require *urgent* referral for endoscopy for investigation of stomach and oesophageal cancer
* All patients who've got **dysphagia**
* All patients who've got an **upper abdominal mass** consistent with stomach cancer
* Patients aged \>= 55 years who've got **weight loss**, AND any of the following:
* upper abdominal pain
* reflux
* dyspepsia
79
which patients require *non urgent* referral for endoscopy for investigation of stomach and oesophageal cancer
* Patients with **haematemesis**
* Patients aged \>= 55 years who've got:
* **treatment-resistant dyspepsia** or
* upper abdominal pain with low haemoglobin levels or
* **raised platelet count** with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
* nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
80
what conditions are associated with H. pylori infection
* peptic ulcer disease
* 95% of duodenal ulcers
* 75% of gastric ulcers
* gastric cancer
* B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
* atrophic gastritis
81
management of H. pylori infection
* a 7-day course of
* a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
* if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
82
how do you diagnose H.pylori infection
Urea breath test
* patients consume a drink containing carbon isotope 13 (13C) enriched urea
* urea is broken down by *H. pylori* urease
* after 30 mins patient exhale into a glass tube
* mass spectrometry analysis calculates the amount of 13C CO2
* should not be performed within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
* sensitivity 95-98%, specificity 97-98%
* may be used to check for *H. pylori* eradication
83
indications for upper GI endoscopy in GORD
* age \> 55 years
* symptoms \> 4 weeks or persistent symptoms despite treatment
* dysphagia
* relapsing symptoms
* weight loss
84
how do you treat endoscopically proved oesophagitis
* full dose proton pump inhibitor (PPI) for 1-2 months
* if response then low dose treatment as required
* if no response then double-dose PPI for 1 month
85
how do you treat endoscopically negative oesophagitis
* full dose PPI for 1 month
* if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
86
what is the histological change seen in barrett's oesophagus
squamous epithelium being replaced by columnar epithelium.
87
how can you subdivide barrett's oesophagus?
short (\<3cm) and long (\>3cm). The length of the affected segment correlates strongly with the chances of identifying metaplasia
88
management of barrett's oesophagus
* Endoscopic surveillance
* for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
* If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
* endoscopic mucosal resection
* radiofrequency ablation
89
management of barrett's oesophagus
* Endoscopic surveillance
* for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
* If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
* endoscopic mucosal resection
* radiofrequency ablation
90
what is the inheritance pattern of haemochromatosis
autosomal recessive
91
what is the prevalence of haemochromatosis in people of european descent
1 in 200, making it more common than cystic fibrosis
92
features of haemochromatosis
* early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
* 'bronze' skin pigmentation
* diabetes mellitus
* liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
* cardiac failure (2nd to dilated cardiomyopathy)
* hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
* arthritis (especially of the hands)
93
which features of haemochromatosis are reversible and which are not
94
what do joint x rays show in haemochromatosis
Joint x-rays characteristically show chondrocalcinosis
95
what do iron studies show in haemochromatosis
* transferrin saturation \> 55% in men or \> 50% in women
* raised ferritin (e.g. \> 500 ug/l) and iron
* low TIBC
96
what are diagnostic tests in haemochromatosis
* transferrin saturation \> 55% in men or \> 50% in women
* raised ferritin (e.g. \> 500 ug/l) and iron
* low TIBC
97
what is the management of haemochromatosis
* Venesection is the first-line treatment
* transferrin saturation should be kept below 50%
* serum ferritin concentration should be kept below 50 ug/l
* desferrioxamine may be used second-line
98
where is haemorrhoidal tissue found
Haemorrhoidal tissue are vascular cushions that contribute to continence
they are found at 3 o'clock, 7'o'clock and 11 o'clock
99
how do you grade haemorrhoids
100
how do you manage haemorrhoids
* soften stools: increase dietary fibre and fluid intake
* topical local anaesthetics and steroids may be used to help symptoms
* rubber band ligation
* surgery is reserved for large symptomatic haemorrhoids which do not respond to the above
* newer treatments: Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy
101
how do thrombosed external haemorrhoids present and how do you manage them
* typically present with significant pain
* examination reveals a purplish, oedematous, tender subcutaneous perianal mass
* if patient presents within 72 hours then referral should be considered for excision.
* Otherwise patients can usually be managed with stool softeners, ice packs and analgesia.
* Symptoms usually settle within 10 days
102
what are the two types of hiatus hernias
* sliding: accounts for 95% of hiatus hernias, the gastroesophageal junction moves above the diaphragm
* rolling (paraoesophageal): the gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus
103
management of hiatus hernia
* all patients benefit from conservative management e.g. weight loss
* medical management: proton pump inhibitor therapy
* surgical management: only really has a role in symptomatic paraesophageal (rolling) hernias
104
when should you suspect oesophageal rupture
in patients with severe chest pain without cardiac diagnosis and signs suggestive of pneumonia without convincing history, where there is history of vomiting
105
investigation and finding of oesophageal rupture
Erect CXR shows infiltrate or effusion in 90% of cases
106
causes for dysphagia
107
extrinsic causes of dysphagia
* mediastinal masses
* cervical spondylosis
108
causes for dysphagia in the oseophageal wall
* Achalasia
* Diffuse oesophageal spasm
* Hypertensive lower oesophageal sphincter
109
intrinsic causes of dysphagia
* Tumours
* Strictures
* Oesophageal web
* Schatzki rings
110
neurological causes of dysphagia
* CVA
* Parkinson's disease
* Multiple Sclerosis
* Myasthenia Gravis
111
six causes of hyposplenism
* splenectomy
* sickle-cell
* coeliac disease
* Graves' disease
* systemic lupus erythematosus
* amyloid
112
what is the difference between acute and chronic diarrhoea
* diarrhoea is \> watery stools per day
* chronic is \>14 days
* acute is \<14 days
113
clinical features of infectious mononucleosis
* sore throat
* pyrexia
* lymphadenopathy
* palatal petychia
* splenomegaly (50%)
* hepatitis (transient rise in ALT)
* lymphocytosis
* maculopapular rash if they take amoxicillin at the same time
114
how long does infectious mononucleosis normally last
symptoms usually resolve within 2-4 weeks
115
management of infectious mononucleosis
* supportive
* lots of fluids
* lots of analgesia
* avoid contact sport for 4 weeks after
116
management of infectious mononucleosis
* supportive
* lots of fluids
* lots of analgesia
* avoid contact sport for 4 weeks after
117
why do you get oxalate renal stones in crohns
impaired bile acid rebsorption increases the loss calcium in the bile. Calcium normally binds oxalate.
doesn't happen in UC as bile is reabsorbed in the ileum
118
compare ulcerative colitis in terms of: features, extra-intestinal features, complications, histology, endoscopy and radiology
119
how do you monitor disease activity in crohn's
CRP
120
what would you see on small bowel enema in crohn's
* high sensitivity and specificity for examination of the terminal ileum
* strictures: 'Kantor's string sign'
* proximal bowel dilation
* 'rose thorn' ulcers
* fistulae
121
management of crohn's
* **Stopping smoking is a priority**
* inducing remission
* **glucocorticoids** (oral, topical or IV)
* **5-ASA drugs** (e.g. **mesalazine**) are used second-line to glucocorticoids but are not as effective
* maintaining remission
* **azathioprine or mercaptopurine** is used first-line to maintain remission
* **surgery**
* segmental bowel resections
* incision and drainage of perianal abscesses
122
what is the peak age of ulcerative colitis
15-25 years and in those aged 55-65 years.
123
where does ulcerative colitis occur in the GI tract
starts at rectum (hence this is the most common site for UC), never spreads beyond ileocaecal valve and is continuous
124
what are the investigations for ulcerative colitis
* colonoscopy and biopsy for diagnosis
* however there is high risk of perforation in severe disease so flexible sigmoidoscopy is preferred
* Barium enema
125
what do you find on endoscopy in ulcerative colitis
* red, raw mucosa, bleeds easily
* no inflammation beyond submucosa
* widespread superficial ulceration which has the appearance of polyps ('pseudopolyps')
* inflammatory cell infiltrate in lamina propria
* neutrophils migrate through the walls of glands to form crypt abscesses
* depletion of goblet cells and mucin from gland epithelium
126
what do you see on barium enema of ulcerative colitis
* loss of haustrations
* superficial ulceration, 'pseudopolyps'
* long standing disease: colon is narrow and short -'drainpipe colon'
127
name some extra-intestinal disease features that are common to both ulcerative colitis and crohn's
* arthritis (most common in both CD and UC)
* erythema nodosum
* episcleritis (more common in CD)
* osteoporosis
* uveitis (much more common in UC)
* pyoderma gangrenosum
* clubbing
* PSC (much more common in UC)
128
how do you grade the severity of a flare of ulcerative colitis
* Mild
* fewer than 4 stools per day
* no systemic disturbance
* normal CRP and ESR
* Moderate
* 4-6 stools per day
* minimal systemic disturbance
* Severe
* more than 6 stools per day
* some evidence of systemic disturbance
* tachycardia
* abdominal tenderness
* anaemia
* fever
* hypoalbuminaemia
129
how do you induce remission in ulcerative colitis
130
how do you maintain remission in ulcerative colitis
131
what is the aetiology of hepatic encephalopathy
not fully understood but involves excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut
132
how do you grade hepatic encephalopathy
* Grade I: Irritability
* Grade II: Confusion, inappropriate behaviour
* Grade III: Incoherent, restless
* Grade IV: Coma
133
how is hepatic encephalopathy treated
lactulose with rifaximin for the secondary prophylaxis of hepatic encephalopathy
* lactulose promotes excretion of ammonia
* antibiotics such as rifaximin modulate the gut flora resulting in decreased ammonia production
134
what is the definition of malnutrition
* a BMI of less than 18.5; or
* unintentional weight loss greater than 10% within the last 3-6 months; or
* a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
135
what is the most common type of oesophageal cancer
* Until recently it was squamous cell carcinoma
* Adenocarcinoma is now the most common type of oesophageal cancer
* Adenocarcinoma is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett's.
136
what is the difference between squamous cell carcinomas and adenocarcinomas of the oesophagus with reference to their epidemiology, location and risk factors
137
presenting features of oesophageal cancer
* dysphagia: the most common presenting symptom
* anorexia and weight loss
* vomiting
* other possible features include: odynophagia, hoarseness, melaena, cough
138
how do you diagnose oesophageal cancer
* endoscopy and biopsy
* CT chest abdo pelvis for initial staging
139
management of oesophageal cancer
* Operable disease is managed by surgery
* Most common is an Ivor-Lewis type oesophagectomy
* The biggest challenge is anastomotic leak - an intrathoracic anastomosis resulting in mediastinitis
* In addition to surgical resection many patients will be treated with adjuvant chemotherapy
140
gastric cancer symptoms
* epigastric pain
* dysphagia (especially if cancer in proximal stomach)
* dyspepsia
* weight loss
* anorexia
* overt upper GI bleeding in a minority
* if lymphatic spread
* virchow's node (left supraclavicular lymph node)
* periumbilical nodule
141
what investigations for gastric cancer
* diagnosis: endoscopy with biopsy
* Signet ring cells may be seen in gastric cancer.
* Higher numbers of signet ring cells are associated with a worse prognosis
* staging: CT
142
what is Courvoisier's law
* Courvoisier's law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
143
presenting features of pancreatic cancer
* classically painless jaundice
* pale stools, dark urine, and pruritus
* cholestatic liver function tests
* however, patients typically present in a non-specific way:
* anorexia
* weight loss
* epigastric pain
* loss of exocrine function (e.g. steatorrhoea)
* loss of endocrine function (e.g. diabetes)
* atypical back pain is often seen
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oesophageal causes of gi bleeding
mallory weiss tear
oesophageal varices
oesophageal cancer
oesophagitis
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gastric causes of gi bleeding
dieulafoy lesion
gastric cancer
gastric ulcer
diffuse erosive gastritis
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duodenal causes of gi bleeding
Duodenal ulcer - erosion of gastroduodenal artery
Aorto-enteric fistula - can be de-novo but usually secondary to an abdominal aortic aneurysm repair
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two risk assessment scores for upper GI bleeding
**Glasgow-Blatchford bleeding score** (**GBS**) is a [screening tool](https://en.wikipedia.org/wiki/Screening_(medicine)) to assess the likelihood that a person with an acute [upper gastrointestinal bleeding](https://en.wikipedia.org/wiki/Upper_gastrointestinal_bleeding) (UGIB) will need to have medical intervention such as a [blood transfusion](https://en.wikipedia.org/wiki/Blood_transfusion) or [endoscopic](https://en.wikipedia.org/wiki/Oesophagogastroduodenoscopy) intervention
**Rockall risk scoring system** attempts to identify patients at risk of adverse outcome following acute [upper gastrointestinal bleeding](https://en.wikipedia.org/wiki/Upper_gastrointestinal_bleeding) - it's for after they've had their endoscopy
148
what does intrinsic factor help to absorb
vit b12
149
which cells secrete intrinsic factor
parietal cells in the stomach
150
causes of b12 deficiency
* pernicious anaemia: most common cause
* post gastrectomy
* vegan diet or a poor diet
* disorders/surgery of terminal ileum (site of absorption)
* Crohn's: either diease activity or following ileocaecal resection
* metformin (rare)
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features of vitamin b12 deficiency
* macrocytic anaemia
* sore tongue and mouth
* neurological symptoms
* the dorsal column is usually affected first (joint position, vibration) prior to distal paraesthesia
* neuropsychiatric symptoms: e.g. mood disturbances
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what is the management for b12 deficiency in those who have no neurological involvement
* Initially administer hydroxocobalamin 1 mg intramuscularly three times a week for 2 weeks.
* The maintenance dose depends on whether the deficiency is diet related or not. For people with B12 deficiency that is:
* *Not* thought to be diet related — administer hydroxocobalamin 1 mg intramuscularly every 2–3 months for life.
* vegans may need this too
* Thought to be diet related — advise people either to take oral cyanocobalamin tablets 50–150 micrograms daily between meals, or have a twice-yearly hydroxocobalamin 1 mg injection.
* advice on diet - eggs and meat
IF THEY'RE ALSO FOLATE DEFICIENT THEN TREAT THE B12 DEFICIENCY FIRST OTHERWISE YOU COULD CAUSE SUBACUTE COMBINED DEGENERATION OF THE CORD
153
what is the management of B12 deficiency in people with neurological features
initially administer hydroxocobalamin 1 mg intramuscularly on alternate days until there is no further improvement,
then administer hydroxocobalamin 1 mg intramuscularly every 2 months.
154
what is the triad for wernicke's encephalopathy
ophthalmoplegia/nystagmus, ataxia and confusion
155
what causes wernicke's encephalopathy
thiamine deficiency which is most commonly seen in alcoholics
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what is korsakoff's syndrome
* when wernicke's (thiamine deficiency) is untreated you can get korsakoff's as well
* it's the addition of anteretrograde amnesia and confabulation
* therefore the features of wernicke-korsakoff's are:
* opthalmaplegia
* nystagmus
* ataxia
* confusion
* anteretrograde amnesia
* confabulation
157
what is the cancer marker for pancreatic cancer
ca19-9
158
what is the cancer marker for hepatocellular carcinoma
alpha fetoprotein
159
management of c difficile
First episode: oral vancomycin
Second or subsequent episode of infection: oral fidaxomicin
160
management of campylobacter enteritis
Clarithromycin
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managment of shigellosis
Ciprofloxacin
162
managment of salmonella
Ciprofloxacin
